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REPATRIATION MEDICAL AUTHORITY STATEMENT
RE: INVESTIGATION INTO HELICOBACTER PYLORI INFECTION
The Repatriation Medical Authority has decided not to make statements of principles
under subsections 196B (2) or (3) in respect of Helicobacter pylori infection, following
notice of an investigation to find out whether a Statement of Principles may be
determined in respect of Helicobacter pylori infection gazetted on 10 September 1997 in
the Commonwealth of Australia Gazette.
Background to the Investigation
The Repatriation Medical Authority of its own initiative under section 196B(4) of the
Veterans’ Entitlements Act 1986 decided to investigate whether a Statement of
Principles may be determined in respect of Helicobacter pylori infection. The
investigation notice was signed by the Chairman of the Repatriation Medical Authority
on 27 August 1997 and was gazetted in accordance with section 196G of the Act in the
Commonwealth of Australia Gazette on 10 September 1997. Submissions were invited
from persons and organisations wishing to make a submission by 31 October 1997.
Helicobacter pylori infection has been determined to be a cause of some diseases, in
some Statements of Principles previously made by the Repatriation Medical Authority.
Submissions received by the Authority pursuant to section 196F
(a) Repatriation Commission provided a detailed referenced submission, together with
copies of the referenced articles, which were received by the Authority on 31 October
1997.
(b) Mr Neil Rogers, Senior Pensions Officer and Advocate, RSL Queensland Branch,
informed the Repatriation Medical Authority by letter faxed to the Secretariat on 1
December 1997 of an intention to provide a late submission, but on 2 December 1997
he informed the Secretariat he would not be doing so.
(c) No other submissions were received pursuant to this section.
Evidence/Information Available to the Repatriation Medical Authority
a.
b.
c.
d.
Submission from Repatriation Commission received 31 October 1997.
Literature search using Medline.
Medical or scientific publications as set out in the bibliography hereto.
Draft Submission prepared for presentation to the Authority by a medical officer
from the Secretariat in conjunction with a member of the Authority.
Reasons for the decision
Page 1 of 14
Helicobacter pylori colonises the mucous layer overlying gastric or gastric-type
metaplastic gut epithelium. Colonisation takes place largely in childhood. No
environmental reservoir has been identified, suggesting a person-to-person method of
transmission. The exact mode/s of transmission have not been determined, but it has
been postulated that faeco-oral, oro-oral, gastro-oral modes of transmission are all
possible. 1 Gastro-oral transmission appears to be the most likely mechanism from
handling of achlorhydric vomitus of newly infected subjects (who are usually children)
or saliva contaminated by gastric contents containing Helicobacter pylori bacteria.
In most infected individuals, infection lasts lifelong
develop gastric atrophy.
2
unless treated or the subjects
The prevalence of Helicobacter pylori infection has shown an inverse relationship with
socio-economic status. The prevalence of Helicobacter pylori infection has decreased in
subsequent cohorts with improvement in the socio-economic status. A number of
studies have shown an association with overcrowding particularly in childhood which is
closely associated with socio-economic status. In the third world countries the
prevalence of Helicobacter pylori infection may reach 70 percent or more. In Western
populations from developed countries the prevalence is lower, rising with age to about
50% at 50 years of age. A decline in childhood infection rates with improving socioeconomic status is likely to be accompanied by an increase in the rate of newly acquired
infections in adulthood, due to an increase in the number of susceptible adults. 3 4 5 6 7
Seroconversion rates indicative of newly acquired Helicobacter pylori infection among
adults is very low. Reported figures are less than one percent per person-year, with
developed countries reporting less than 0.5 percent per person-year. There is limited
evidence that some gastroenterologists who perform upper endoscopies and
institutionalised populations may be at higher risk of acquisition of Helicobacter pylori
colonization. Person-to-person transmission between spouses does not seem to occur
readily. Transmission of Helicobacter pylori by fibroscope and gastroduodenoscopies
have been reported. 8 9 10 11 12 13 14 15 16 17 18
Vincent P (1995) Transmission and acquisition of Helicobacter pylori infection: evidences and
hypothesis. Biomedicine & Pharmacotherapy. Vol 49 No 1 p 13.
2 NIH consensus development panel on Helicobacter pylori in Peptic Ulcer Disease (1994)
Helicobacter pylori in peptic ulcer disease. JAMA Vol 272 pp 65-69.
3 Vincent P (1995) Transmission and acquisition of Helicobacter pylori infection: evidences and
hypothesis. Biomedicine & Pharmacotherapy. Vol 49 No 1 pp 13-14.
4 The EUROGAST Study Group (1993) Epidemiology of, and risk factors for, Helicobacter pylori
infection among 3194 asymptomatic subjects in 17 populations. Gut Vol 34 No 12 pp 1672-1676.
5 Mendall MA and Northfield TC (1995) Transmission of Helicobacter pylori infection. Gut Vol
37 No 1 pp 1-3.
6 Lindkvist P, Asrat D, Nilsson I, Tsega E, Olsson GL, Wretlind B and Giesecke J (1996) Age at
acquisition of Helicobacter pylori infection: comparison of a high and a low prevalence country.
Scandinavian Journal of Infectious Diseases Vol 28 No 2 pp 181-184.
7 Banatvala N, Mayo K, Megraud F, Jennings R, Deeks JJ and Feldman RA (1993) The cohort
effect and Helicobacter pylori. J Infect Dis Vol 168 No 1 pp 219-221.
8 Vincent P (1995) Transmission and acquisition of Helicobacter pylori infection: evidences and
hypothesis. Biomedicine & Pharmacotherapy. Vol 49 No 1 pp 13-14.
1
Page 2 of 14
Evidence does not support increased risk of acquisition of Helicobacter pylori infection
in military personnel in recent times. 19 20 21
In the vast majority of subjects Helicobacter pylori infection does not cause any specific
symptoms. However, it has been recognised as an important risk factor for gastritis,
peptic ulcer disease and malignant neoplasm of the stomach. The National Institute of
Health Consensus Development Conference on Helicobacter pylori in peptic ulcer
disease concluded that the data are not sufficient to support prophylactic antimicrobial
therapy to prevent ulcer disease or gastric neoplasia in asymptomatic patients. 22 23 24 25
Veldhuyzen van Zanten SJ, Pollak PT, Best LM, Bezanson GS and Marrie T (1994) Increasing
prevalence of Helicobacter pylori infection with age: continuous risk of infection in adults rather
than cohort effect. Journal of Infectious Diseases Vol 169 No 2 pp 434-437.
10 Perez-Perez GI, Witkin SS, Decker MD and Blaser MJ (1991) Seroprevalence of Helicobacter
pylori in couples. J Clin Microbiol Vol 29 No 3 pp 642-644.
11 Parsonnet J, Blaser MJ, Perez-Perez GI, Hargrett-Bean N and Tauxe RV (1992) Symptoms and
risk factors of Helicobacter pylori infection in a cohort of epidemiologists. Gastroenterology Vol
102 No 1 pp 41-46.
12 Goodman KJ and Correa P (1995) The transmission of Helicobacter pylori. A critical review of
the evidence. International Journal of Epidemiology Vol 24 No 5 pp 875-887.
13 Cullen DJ, Collins BJ, Christiansen KP, Epis J, Warren JR, Surveyor I and Cullen KJ (1993)
When is Helicobacter pylori infection acquired? Gut Vol 34 No 12 pp 1681-1682.
14 Berkowicz J and Lee A (1987) Person-to-person transmission of Campylobacter pylori. Lancet
Vol 2 pp 680-681.
15 Langenberg W, Rauws EA, Oudbier JH and Tygat GNJ (1990) Patient-to-patient transmission
of Campylobacter pylori infection by fibreoptic gastroduodenoscopy and biopsy. J Infect Dis
Vol 161 pp 507-511.
16 Böhmer CJ, Klinkenberg-Knol EC, Kuipers EJ, Niezen-de Boer MC, Schreuder H, SchuckinkKool F and Meuwissen SG (1997) The prevalence of Helicobacter pylori infection among
inhabitants and healthy employees of institutes for the intellectually disabled. American Journal
of Gastroenterology, Vol.92(6), pp. 1000-4.
17 Harris AW, Douds A, Meurisse EV, Dennis M, Chambers S and Gould SR (1995).
Seroprevalence of Helicobacter pylori in residents of a hospital for people with severe learning
difficulties. European Journal of Gastroenterology & Hepatology 7 (1) pp 21-23.
18 Fawcett JP, Shaw JP, Cockburn M, Brooke M and Barbezat GO (1996). Seroprevalence of
Helicobacter pylori in a birth cohort of 21 year old New Zealanders. European Journal of
Gastroenterology & Hepatology 8 (4) pp 365-9.
19 Hyams KC, Taylor DN, Gray GC, Knowles JB, Hawkins R and Malone JD (1995) The risk of
Helicobacter pylori infection among U.S. military personnel deployed outside the United States.
American Journal of Tropical Medicine & Hygiene Vol 52 No 1 pp 109-112.
20 Hammermeister I, Janus G, Schamarowski F, Rudlolf M, Jacobs E and Kist M (1992) Elevated
risk of Helicobacter pylori infection in submarine crews. Eur J Clin Microbiol Infect Dis Vol 11
pp 9-14.
21 Basso L, Beattie S, Lawlor S, Clune J and O'Morain C (1994) A descriptive follow-up study on
Helicobacter pylori infection before and after exposition to a war area. European Journal of
Epidemiology Vol 10 No 1 pp 109-111.
22 NIH consensus development panel on Helicobacter pylori in Peptic Ulcer Disease (1994)
Helicobacter pylori in peptic ulcer disease. JAMA Vol 272 pp 65-69.
23 The EUROGAST Study Group (1993) Epidemiology of, and risk factors for, Helicobacter
pylori infection among 3194 asymptomatic subjects in 17 populations. Gut Vol 34 No 12 pp
1672-1676.
24 Taylor DN and Blaser MJ (1991) The epidemiology of Helicobacter pylori infection.
Epidemiologic Reviews Vol 13 pp 42-59.
25 Davis S (1996) Triple therapy and Helicobacter pylori. Aust Fam Phys Vol 25 No 1 pp 53-59.
9
Page 3 of 14
The Repatriation Medical Authority considered and had regard to the provisions of the
Act and in particular, sections 5AB(2) (‘sound medical-scientific evidence’), 5D
(‘disease’), 8 (‘war caused death’), 9 (‘war caused injuries or diseases’), and Part XIA.
(i)
The RMA considered the definition of ‘disease’ in s. 5D which is as follows:
“(1) In this Act, unless the contrary intention appears:
‘disease’ means:
(a)
any physical or mental ailment, disorder, defect or morbid
condition (whether of sudden onset or gradual development); or
(b)
the recurrence of such an ailment, disorder, defect or
morbid condition;
but does not include:
(c)
the aggravation of such an ailment, disorder, defect or
morbid condition; or
(d)
a temporary departure from:
(i)
the normal physiological state; or
(ii) the accepted ranges of physiological or biochemical
measures;
that results from normal physiological stress (for example, the effect
of exercise on blood pressure) or the temporary effect of extraneous
agents (for example, alcohol on blood cholesterol levels);”
(ii)
The RMA had regard to the definition of ‘disease’ for the purposes of the
Safety Rehabilitation and Compensation Act 1988 , as follows:
“disease means:
(a) any ailment suffered by an employee; or
(b) the aggravation of any such ailment;
being an ailment or an aggravation that was contributed to in a
material degree by the employee’s employment by the
Commonwealth or a licensed corporation”.
(iii)
Whilst the RMA noted that the definitions are not the same, it considered
that sufficient similarity existed to warrant regard to interpretations of the
definition of ‘disease’ in the SRC Act.
(iv)
The RMA had regard to the consideration of the definition of disease for the
purpose of the SRC Act in Comcare v Mooi (1996) 42 ALD 495. There
Drummond J. of the Federal Court, held that particular facts and
circumstances would only be caught by the statute if they fell within the
defining phrase and also within the ‘connotations which the word defined by
that phrase has in ordinary speech”.
Page 4 of 14
(v)
Accordingly, applying that reasoning to the definition of ‘disease’ in s. 5D,
the RMA formed the opinion it would not be enough for a person to say that
a condition they were suffering from was a ‘defect’ in one or more meaning
of that word, or ailment, disorder, or morbid condition if there was
otherwise no connotation of disease in its ordinary usage. Having regard to
the definition, the RMA also formed the opinion that the definition was not
intended to include those conditions as a disease that involve only a
temporary departure from the normal range of measurements. Such
exclusions provided a negative yardstick to assist in the interpretation of
what is meant by ‘disease’ and the RMA acknowledged that in considering
such exclusions it apply objective medical and scientific standards to its
consideration.
(vi)
The RMA was familiar with the ordinary English meaning of ailment,
disorder, defect or morbid condition, which terms are used in s.5D, and
considered whether Helicobacter pylori infection was within the ordinary
meaning of these terms and applied the ordinary meaning of those terms to
its consideration of whether Helicobacter pylori infection is a disease.
(vii)
In considering whether Helicobacter pylori infection was a ‘disease’ for the
purposes of the VEA, the RMA also relied upon its expert medical
knowledge.
Decision
At its meeting on 3 March 1998, the Repatriation Medical Authority, decided not to
make a Statement of Principles in respect of Helicobacter pylori infection for the
purposes of subsection (2) or (3) of s.196B of the Act.
Page 5 of 14
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